The heart has four valves which ensure forward flow of incoming blood to the systemic circulation. The left side has the mitral valve which is positioned between the left atrium and left ventricle and the aortic valve which is located at the junction of the left ventricular outflow tract and the aortic root. The function of these two valves is to ensure that oxygenated blood from the lung continues to flow into aortic root through the left side of the heart in a forward direction. In the right side of the heart, there are two similar valves called the tricuspid valve and the pulmonary valve.
These four valves are entirely passive structures which neither consume energy nor contract dynamically. These valves are composed of leaflets which passively open and close dictated by the pressure difference created. The mitral and tricuspid valves are called atrioventricular valves since they are located between atrium and ventricle. The mitral valve is composed of two leaflets and the tricuspid valve is composed of three leaflets. The aortic and pulmonary valves are called semilunar cusps since the leaflets are semilunar in shape. Both of the aortic and pulmonary valves have three cusps.
Heart valves may be affected by abnormality in structure and function by congenital or acquired valve disorder. Congenital valve abnormalities may either manifest with life-threatening disorder at birth or remain latent until mid life or even later in life. Acquired disorders are frequently caused by conditions such as rheumatic fever, degenerative disorder, infection or trauma.
Severe aortic regurgitation may be caused by aortic dissection, in which case aortic valve replacement is usually required. In addition, serious aortic regurgitation may also occur as a result of rheumatic or degenerative valvular disease. The mainstay of prosthetic valves used in aortic valve disease is so called mechanical valve and tissue valves, both of the stented type. The leaflets of mechanical valves are constructed of pyrolitic carbon material encased in a titanium housing. Tissue valves are composed of materials derived from animal tissue. Tissue valves are commonly constructed over a skeletal frame of titanium with an outer sewing rim to facilitate suture implantation. The valve material per se may either come from bovine pericardium or from the porcine aortic valve treated in glutaraldehyde. These prosthetic apparatus are implanted in the patients' aortic annulus after the diseased aortic leaflets have been removed.
To prevent thrombotic complications after a mechanical valve implantation, lifelong anticoagulation is essential. Even with anticoagulation, patients could still experience bleeding or thrombotic complications. On the other hand, tissue valves are generally free of such complications, obviating anticoagulation, but tissue valves have relatively limited durability compared to mechanical valves. As a result these patients require future reoperation. To overcome the limitations of these different types of artificial valves, a durable method of aortic valve restoration is desirable. However, at present aortic valve repair is considered feasible in only certain selected situations.
The aortic root not only serves as a simple passage for blood, but it is also a highly sophisticated elastic structure which allow cyclic expansion of the aortic diameter to as much as 30% of its basal diameter according to the rhythmic changes of the cardiac cycle. Since this structure is sustained under very high blood pressures, most of the existing methods of aortic valve repair unable to withstand the associated mechanical stress are prone to failure and relapse.
The three major factors to preserve the function of the aortic valve include maintaining the appropriate diameter of the sinotubular junction and the aortic annulus, and state of the leaflets per se. Only when the functions of these three factors are optimally recovered, the aortic valve function can be successfully restored. Existing methods to repair the aortic valve haven't met these requirements entirely. For example, resuspension of the aortic valve leaflets inside an artificial vascular conduit has been suggested as an effective method of repairing ascending aortic aneurysm due to Marfan syndrome with morphologically normal aortic leaflets (David T. E. ‘Aortic valve repair in patients with Marfan syndrome and ascending aorta aneurysms due to degenerative disease’ J. Card. Surg. 1994; 9(2 Suppl): 182-7). However, this method is applicable only to limited situations. One drawback is that the sinus portion in the proximal aortic root has to be removed. Furthermore, this method may lead to serious bleeding complications in aortic dissection as sutures are passed through friable and edematous tissue.
Another surgical method applicable to Marfan patients, is replacement of aneurysmal ascending aortic tissue with a suitably tailored segment of a vascular conduit (Sndro Gelsomino et al. ‘A short-term experience with the Tirone David I valve sparing operation for the treatment of aneurysms of the ascending aorta and aortic root’ Cardiovascular Surgery 2003; 11(3): 189-194; Kallenbach K. et al. ‘Results of valve-sparing aortic root reconstruction in 158 consecutive patients’ Ann. Thorac. Surg. 2002; 74(6): 2026-32). However, this method is also prone to serious bleeding in aortic dissection or even in simple aneurysms in these patients. Furthermore, this method also shares the same drawback having to remove the function of the native sinus of Valsalva.
In contrast to these methods, replacement of the dysfunctional valve leaflets with glutaraldehyde fixed autologous pericardium may appear to correct the problem of aortic regurgitation (Riyadh Cardiac Centre, Armed Forces Hospital, Kingdom of Saudi Arabia. ‘Aortic valve repair using bovine pericardium for cusp extension’ J. Thorac. Cardiovasc. Surg. 1988; 96(5): 760-4; Cosgrove D. M. et al. ‘Valvuloplasty for aortic insufficiency’ J. Thorac. Cardiovasc. Surg. 1991; 102(4): 571-6; Haydar H. S. at al. ‘Valve repair for aortic insufficiency: surgical classification and techniques’ Eur. J. Cardiothorac. Surg. 1997; 11(2): 258-65), but in the long term, leaflet coaptation will eventually fail as this function is dictated by the diameters of the sinotubular junction and the aortic annulus, both of which may progressively increase.